A team of Rockefeller scientists have found that a plasma component normally involved in vascular health, blood clotting and inflammation may play a role in the development of Alzheimer’s disease (AD). A plasma protein, called Factor XII, is part of a cascade of enzymes that induces blood coagulation and inflammation and that can be activated by beta-amyloid, a molecule that forms sticky plaques in the brains of Alzheimer’s patients. To take out Factor XII, the research team used a molecule in mice that prevented the gene from making the protein. Normally, mice show much greater brain inflammation than healthy mice. However, AD mice whose Factor XII had been knocked down had much less inflammation than untreated AD mice and had brains that were more similar to those of healthy mice. Further, the researchers conducted behavioral studies of AD mice with reduced Factor XII and showed that their cognitive function improved. The research contributes to the increasing evidence that vascular abnormalities are playing an important role in the cognitive decline and inflammation in some AD patients.